Cell interactions in the sea urchin embryo studied by fluorescence photoablation

Science ◽  
1990 ◽  
Vol 248 (4959) ◽  
pp. 1115-1118 ◽  
Author(s):  
C. Ettensohn
Keyword(s):  
Sea Urchin ◽  
Cell Interactions ◽  
Sea Urchin Embryo

Cell interactions and mesodermal cell fates in the sea urchin embryo

Development ◽  
1992 ◽  
Vol 116 (Supplement) ◽  
pp. 43-51 ◽  
Author(s):  
Charles A. Ettensohn
Keyword(s):  
Sea Urchin ◽  
Cell Interactions ◽  
Cell Labeling ◽  
Cell Fates ◽  
Mesodermal Cell ◽  
Sea Urchin Embryo ◽  
Present Information ◽  
Cell Type Specific ◽  
Mesenchyme Cells

Cell interactions during gastrulation play a key role in the determination of mesodermal cell fates in the sea urchin embryo. An interaction between primary and secondary mesenchyme cells (PMCs and SMCs, respectively), the two principal populations of mesodermal cells, regulates the expression of SMC fates. PMCs are committed early in cleavage to express a skeletogenic phenotype. During gastrulation, they transmit a signal that suppresses the skeletogenic potential of a subpopulation of SMCs and directs these cells into an alternative developmental pathway. This review summarizes present information concerning the cellular basis of the PMC-SMC interaction, as analyzed by cell transplantation and ablation experiments, fluorescent cell labeling methods and the use of cell type-specific molecular markers. The nature and stability of SMC fate switching, the timing of the PMC-SMC interaction and its quantitative characteristics, and the lineage, numbers and normal fate of the population of skeletogenic SMCs are discussed. Evidence is presented indicating that PMCs and SMCs come into direct filopodial contact during the late gastrula stage, when the signal is transmitted. Finally, evolutionary questions raised by these studies are briefly addressed.

Cell Interactions in the Sea Urchin Embryo

1996 ◽  
pp. 47-98 ◽  
Author(s):  
Charles A. Ettensohn ◽  
Kirsten A. Guss ◽  
Katherine M. Malinda ◽  
Roberta N. Miller ◽  
Seth W. Ruffins
Keyword(s):  
Sea Urchin ◽  
Cell Interactions ◽  
Sea Urchin Embryo

scholarly journals Dynamics of thin filopodia during sea urchin gastrulation

Development ◽  
1995 ◽  
Vol 121 (8) ◽  
pp. 2501-2511 ◽  
Author(s):  
J. Miller ◽  
S.E. Fraser ◽  
D. McClay
Keyword(s):  
Sea Urchin ◽  
Positional Information ◽  
Cell Interactions ◽  
Average Growth ◽  
Sea Urchin Embryo ◽  
Ligand Interactions ◽  
Patterning Defect ◽  
Mesenchyme Cell ◽  
Mesenchyme Cells ◽  
Primary Mesenchyme Cells

At gastrulation in the sea urchin embryo, a dramatic rearrangement of cells establishes the three germ layers of the organism. Experiments have revealed a number of cell interactions at this stage that transfer patterning information from cell to cell. Of particular significance, primary mesenchyme cells, which are responsible for production of the embryonic skeleton, have been shown to obtain extensive positional information from the embryonic ectoderm. In the present study, high resolution Nomarski imaging reveals the presence of very thin filopodia (02-0.4 micron in diameter) extending from primary mesenchyme cells as well as from ectodermal and secondary mesenchyme cells. These thin filopodia sometimes extend to more than 80 microns in length and show average growth and retraction rates of nearly 10 microns/minute. The filopodia are highly dynamic, rapidly changing from extension to resorption; frequently, the resorption changes to resumption of assembly. The behavior, location and timing of active thin filopodial movements does not correlate with cell locomotion; instead, there is a strong correlation suggesting their involvement in cell-cell interactions associated with signaling and patterning at gastrulation. Nickel-treatment, which is known to create a patterning defect in skeletogenesis due to alterations in the ectoderm, alters the normal position-dependent differences in the thin filopodia. The effect is present in recombinant embryos in which the ectoderm alone was treated with nickel, and is absent in recombinant embryos in which only the primary mesenchyme cells were treated, suggesting that the filopodial length is substratum dependent rather than being primary mesenchyme cell autonomous. The thin filopodia provide a means by which cells can contact others several cell diameters away, suggesting that some of the signaling previously thought to be mediated by diffusible signals may instead by the result of direct receptor-ligand interactions between cell membranes.

Cell-cell interactions regulate skeleton formation in the sea urchin embryo

Development ◽  
1993 ◽  
Vol 119 (3) ◽  
pp. 833-840 ◽  
Author(s):  
N. Armstrong ◽  
J. Hardin ◽  
D.R. McClay
Keyword(s):  
Sea Urchin ◽  
Cell Interactions ◽  
Sea Urchin Embryo ◽  
Skeletal Pattern ◽  
Tissue Sensitivity ◽  
Mesenchyme Cells ◽  
Larval Skeleton ◽  
Skeleton Formation

In the sea urchin embryo, the primary mesenchyme cells (PMCs) make extensive contact with the ectoderm of the blastula wall. This contact is shown to influence production of the larval skeleton by the PMCs. A previous observation showed that treatment of embryos with NiCl2 can alter spicule number and skeletal pattern (Hardin et al. (1992) Development, 116, 671–685). Here, to explore the tissue sensitivity to NiCl2, experiments recombined normal or NiCl2-treated PMCs with either normal or NiCl2-treated PMC-less host embryos. We find that NiCl2 alters skeleton production by influencing the ectoderm of the blastula wall with which the PMCs interact. The ectoderm is responsible for specifying the number of spicules made by the PMCs. In addition, experiments examining skeleton production in vitro and in half- and quarter-sized embryos shows that cell interactions also influence skeleton size. PMCs grown in vitro away from interactions with the rest of the embryo, can produce larger spicules than in vivo. Thus, the epithelium of the blastula wall appears to provide spatial and scalar information that regulates skeleton production by the PMCs.

Pattern formation during gastrulation in the sea urchin embryo

Development ◽  
1992 ◽  
Vol 116 (Supplement) ◽  
pp. 33-41 ◽  
Author(s):  
David R. McClay ◽  
Norris A. Armstrong ◽  
Jeff Hardin
Keyword(s):  
Sea Urchin ◽  
Spatial Information ◽  
Cell Types ◽  
Cell Interactions ◽  
Pigment Cells ◽  
Original Position ◽  
Embryonic Cells ◽  
Sea Urchin Embryo ◽  
Mesenchyme Cells ◽  
Primary Mesenchyme Cells

The sea urchin embryo follows a relatively simple cell behavioral sequence in its gastrulation movements. To form the mesoderm, primary mesenchyme cells ingress from the vegetal plate and then migrate along the basal lamina lining the blastocoel. The presumptive secondary mesenchyme and endoderm then invaginate from the vegetal pole of the embryo. The archenteron elongates and extends across the blastocoel until the tip of the archenteron touches and attaches to the opposite side of the blastocoel. Secondary mesenchyme cells, originally at the tip of the archenteron, differentiate to form a variety of structures including coelomic pouches, esophageai muscles, pigment cells and other cell types. After migration of the secondary mesenchyme cells from their original position at the tip of the archenteron, the endoderm fuses with an invagination of the ventral ectoderm (the stomodaem), to form the mouth and complete the process of gastrulation. A larval skeleton is made by primary mesenchyme cells during the time of archenteron and mouth formation. A number of experiments have established that these morphogenetic movements involve a number of cell autonomous behaviors plus a series of cell interactions that provide spatial, temporal and scalar information to cells of the mesoderm and endoderm. The cell autonomous behaviors can be demonstrated by the ability of micromeres or endoderm to perform their morphogenetic functions if either is isolated and grown in culture. The requirement for cell interactions has been demonstrated by manipulative experiments where it has been shown that axial information, temporal information, spatial information and scalar information is obtained by mesoderm and endoderm from other embryonic cells. This information governs the cell autonomous behavior and places the cells in the correct embryonic context.

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